The mechanism of acute silver nitrate toxicity in freshwater rainbow trout ( Oncorhynchus mykiss) is inhibition of gill Na + and Cl −1 transport

Abstract

Rainbow trout ( Oncorhynchus mykiss) were exposed to 2 and 10 μg l −1 silver (as AgNO 3) for up to 75 h in moderately hard freshwater. At 10 μg l −1 total Ag, branchial Na + and Cl − influxes were inhibited by over 50% immediately and by almost 100% at 8 h, and showed no signs of recovery over the duration of the experiment. Na + and Cl − effluxes were much less affected. These changes in unidirectional fluxes resulted in a large net loss of both Na + and Cl − across the gills and a significant decrease in plasma [Na +] and [Cl −1]. The effects of exposure to 2 μg l −1 Ag on Na + and Cl −1 transport were generally similar to those at 10 μg l −1, but were of a lesser magnitude. Unidirectional Na + fluxes recovered immediately following removal of silver, after 48 h exposure to 2 μg l −1. Michaelis-Menten kinetic analysis demonstrated that the maximal rate of Na + influx ( J max) was significantly reduced after 48 h exposure to 2 μg l −1 Ag, whereas the affinity of the transport sites for Na + (1/K m) was unaffected, indicating that the inhibition of Na + influx by silver was of a non-competitive nature. Fish exposed to 10 μg l −1 Ag for 48 h also had significantly lower activities of the branchial enzymes Na + K + ATPase (85% inhibition) and carbonic anhydrase (28% inhibition). The results of this study suggest that a disturbance of branchial ionoregulation, as a result of inhibition of branchial enzymes involved in ion transport, is the principal mechanism of the physiological toxicity of silver nitrate to freshwater fish.